| Abstract/Notes |
In part VIII of this series I began my discusson on how disburbances in insulin metabolism can alter brain chemistry, leading to formation of the generally recognized cause of Alzheimer's disease/senile dementia, amyloid beta (AB), commonly known as "amyloid plaques." Furthermore, I pointed out that the research suggesting that AB is a major cause of Alzheimer'sdisease/senile dementia is actually quite controversial and that, instead, aggregates of AB that form neurotoxic soluble oligomers (ABOs) are much more likely causational factors. Next, I presented several quotes from different studies that provided compelling evidence that not only do disburbances in insulin metabolism lead to increased production of ABOs but ABOs can trigger removal of insulin receptors in the brain, suggesting a very potent vicious circle between disturbances of insulin metabolism and existence of the factors most directly linked with Alzheimer's disease/senile dementia development, ABOs.
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